胆汁酸代谢在原发性胆汁性胆管炎发病机制中的作用
DOI: 10.3969/j.issn.1001-5256.2022.10.031
利益冲突声明:所有作者均声明不存在利益冲突。
作者贡献声明:贾皖婷负责文献查找、阅读及文章撰写; 刘晓晓对研究思路有关键贡献; 邰文琳负责文章修改。
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摘要: 原发性胆汁性胆管炎(PBC)是一种胆汁淤积性自身免疫性肝病, 以中老年女性高发, 小胆管淋巴细胞浸润和胆汁淤积为主要特征。临床表现以疲惫和胆汁淤积造成的瘙痒为主。目前被批准的治疗药物熊去氧胆酸和奥贝胆酸, 主要是通过调节胆汁酸代谢,特异且有效的改善胆汁淤积而起作用。本文介绍了胆汁酸生理及疾病状态下的病理改变,归纳了胆汁酸代谢参与疾病发病机制的可能方式,总结了目前针对胆汁酸代谢的疾病治疗方法。指出PBC胆汁酸代谢改变主要与阴离子交换器2缺陷、胆汁酸代谢的转运体和核受体先天遗传变异及后天适应性改变、肠道菌群结构发生改变有关。Abstract: Primary biliary cholangitis (PBC) is a cholestatic autoimmune liver disease characterized by a high incidence rate in middle-aged and elderly women, lymphocyte infiltration in small bile ducts, and cholestasis. Main clinical manifestations include fatigue and pruritus caused by cholestasis. Ursodeoxycholic acid and obeticholic acid are currently approved therapeutic drugs for PBC and exert a therapeutic effect by regulating bile acid metabolism and specifically and effectively improving cholestasis. This article introduces the physiological and pathological changes of bile acids in disease states and summarizes the possible ways in which bile acid metabolism is involved in the pathogenesis of diseases and the current treatment methods for bile acid metabolism. It is pointed out that the changes of bile acid metabolism in PBC are mainly associated with anion exchanger 2 deficiency, innate genetic variation and acquired adaptive changes of bile acid metabolism transporters and nuclear receptors, and changes in the structure of intestinal flora.
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Key words:
- Primary Biliary Cholangitis /
- Bile Acids and Salts /
- Pathologic Processes
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